Abstract

Many of the features of zinc deficiency and of essential fatty acid (EFA) deficiency are similar in both animals and humans. The two agents interact in various ways. EFAs are important in zinc absorption, probably after conversion to prostaglandins (PGs). Zinc seems necessary for at least two stages in EFA metabolism, the conversion of linoleic acid to gamma-linolenic acid, and the mobilisation of dihomogammalinolenic acid (DGLA) for the synthesis of 1 series PGs. Zinc may also be important in the conversion of DGLA to arachidonic acid and in arachidonic acid mobilisation for 2 series PG formation. These interactions shed considerable light on a number of clinical syndromes, including acrodermatitis enteropathica, total parenteral nutrition, diabetes mellitus, the glucagonoma syndrome and sickle cell anaemia. There is substantial evidence to suggest that anorexia nervosa is due to a combined deficiency of zinc and EFAs. Understanding of the roles of zinc and EFAs in these various clinical situations is likely to lead to improved therapy.